RESUMO
Objective To investigate the inhibitory effect of naringin (NAR) on proliferation and apoptosis of Eca109 esophageal cancer cells and its mechanism. Methods Eca109 cells were cultured with 0, 15, 30, 45 µmol/L NAR treatment for 24, 48 and 72 hours. The colony forming ability of Eca109 esophageal cancer cells was evaluated by cell colony forming assay, the cell proliferation activity was detected by MTT assay, and the invasion ability of cancer cells was detect by TranswellTM assay; Apoptosis was detected by annexin V-FITC/PI double labeling combined with flow cytometry. Western blot analysis was used to detect the protein expression of B-cell lymphoma factor 2 (Bcl2), Bcl2 related X protein (BAX), cytochrome C (CytC), caspase-3, caspase-9, Janus kinase 2 (JAK2), phosphorylated JAK2 (p-JAK2) and signal transducer and activator of transcription 3 (STAT3), phosphorylated STAT3 (p-STAT3), protein kinase B (AKT), phosphorylated AKT(p-AKT). Results NAR inhibited the proliferation and colony formation of Eca109 cells, suppressed the invasion of Eca109 cells and promoted the apoptosis of Eca109 cells; NAR promoted the expression of BAX, CytC, caspase-3, caspase-9, p-STAT3, p-AKT, AKT and p-JAK2 and inhibited the expression of Bcl2. Conclusion NAR can inhibit the proliferation, invasion, and colony formation of Eca109 cells and promote its apoptosis by blocking the activation of JAK/STAT signal pathway.
